Our Microbiome Minute series returns, where experts from the AGA Center for Gut Microbiome Research & Education break down the most interesting research developments in this space with 1-minute summaries.
Dr. Phillip Tarr, chair of AGA’s microbiome center, provides a review of the article, “A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation,” published in Gastroenterology by Arivarasu N. Anbazhagan, et al.
Anbazhagan, et al, present a novel monogenic phenotype relevant to IBD. Knockout of the gene encoding putative anion transporter-1 (PAT1, also termed SLC26A6), which mediates intestinal oxalate secretion, causes mice to experience hyperoxaluria and
nephrolithiasis. People with IBD have higher rates of hyperoxaluria and kidney stones, and it is postulated that defects in intestinal excretion of oxalate contributes to this process. In this paper, the authors report the simultaneous presence of a variant (dysbiotic) gut bacterial community, characterized by diminished relative presence of Firmicutes and increased abundance of Bacteroidetes, while Lactobacillus was better represented in the wild type mice. Interestingly, knockout mice transferred their gut microbial communities to their wild type littermates, after which altered gut barrier function in the recipients was identified. In addition to a variant gut microbiome, PAT1 knockout mice displayed increased susceptibility to DSS colitis.
This work provides a model to dissect the intertwined independent variables of gut microbial content, tight junction integrity, gut microbial metabolism, host response to microbial populations and the dependent variable of colitis. Such work could determine which of these processes are within the causal pathway leading to mucosal injury, and which are secondary consequences of organ injury.
Phillip Tarr, MD
Chair, AGA Center for Gut Microbiome Research & Education
